Research advances in portal hypertension in patients with nonalcoholic fatty liver disease / 临床肝胆病杂志

Nonalcoholic fatty liver disease (NAFLD) is often complicated by clinically significant portal hypertension (PHT) during its progression to liver cirrhosis, which is primarily caused by increased intrahepatic vascular resistance. The pathogenesis of PHT in NAFLD remains unclear. This article summarizes the current research status of PHT in NAFLD and related cellular and molecular mechanisms in the development of PHT, in order to provide a theoretical basis for novel preventive and therapeutic strategies for NAFLD.

Pathophysiology of Portal Hypertension, What's New? / 대한소화기학회지

Portal hypertension (PHT) is associated with changes in the intrahepatic, systemic and portosystemic collateral circulations. Alteration in vasoreactivity (vasodilation and vasoconstriction) plays a central role in the pathogenesis of PHT by contributing to increased intrahepatic resistance, hyperdynamic circulation and the expansion of the collateral circulation. PHT is also importantly characterized by changes in vascular structure; termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the sprouting of new blood vessels, also occurs in PHT, especially in the expansion of the portosystemic collateral circulation. These complementary processes of vasoreactivity, vascular remodeling and angiogenesis represent important targets in the research for the treatment of portal hypertension.

Hemodynamic alterations in cirrhosis and portal hypertension / 대한간학회지

Portal hypertension (PHT) is associated with hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation. Increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation play a central role in the pathogenesis of PHT. PHT is also characterized by changes in vascular structure, termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the formation of new blood vessels, also occurs with PHT related in particular to the expansion of portosystemic collateral circulation. The complementary processes of vasoreactivity, vascular remodeling, and angiogenesis represent important targets for the treatment of portal hypertension. Systemic and splanchnic vasodilatation can induce hyperdynamic circulation which is related with multi-organ failure such as hepatorenal syndrome and cirrhotic cadiomyopathy.

Update on the treatment of portal hypertension / 대한내과학회지

Portal hypertension is responsible for most of the complications associated with liver cirrhosis, including variceal hemorrhage, ascites, and hepatic encephalopathy. It has become clear that a decrease in portal pressure can prevent or manage these serious complications. Until now, the pharmacotherapy of portal hypertension has focused on agents that reduce splanchnic blood flow, such as non-selective beta blockers and splanchnic vasoconstrictors. However, recent advances in the knowledge of the pathophysiology of portal hypertension have directed future treatment towards modulating the increased intrahepatic vascular resistance, in addition to managing the splanchnic circulation. Consequently, agents that modulate either the hyperdynamic circulation or angiogenesis are new therapeutic targets for managing portal hypertension. Several have been developed or are under investigation. To incorporate these pharmacologic approaches into clinical practice, data on patient-oriented outcomes are needed.

Pathophysiology and diagnosis of portal hypertension / 대한내과학회지

Portal hypertension (PHT) as a consequence of liver cirrhosis is responsible for serious complications such as variceal bleeding, ascites and hepatic encehphalopathy. PHT is caused by increased intrahepatic vascular resistance and maintained by increased portal venous inflow. Increased intrahepatic vascular resistance has some reversible dynamic components related with activated hepatic stellate cell(HSC) and vacular activation mediators, therefore which come into the spotlight as new targets in treatment of PHT. PHT also induces hyperdynamic circulation by reduced systemic vascular resistance (SVR) and increased cardiac output. The gold-standard method for assessing the severity of PHT is a measurement of the hepatic venous pressure gradient (HVPG). However it is invasive, so non-invasive methods such as Doppler ultrasonography is under investigation as additive method.